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Andres T Blei

Publications and source records attributed to Andres T Blei.

At least 19 recordsLinked to original sources
PubMed2006

Surgically restoring portal blood flow to the liver in children with primary extrahepatic portal vein thrombosis improves fluid neurocognitive ability.

OBJECTIVES: Children with primary extrahepatic portal vein thrombosis (EHPVT) have portal-systemic shunting, which may lead to disturbed neurocognitive function similar to portal-systemic encephalopathy (PSE) seen with chronic liver disease and cirrhosis. The functions most affected are those involving fluid cognitive ability, which comprise neurocognitive domains such as attention, processing speed, and short-term memory, that are particularly vulnerable to systemic illness or diffuse neurologic insult. We determined the fluid cognitive ability of children with EHPVT and whether surgically restoring portal blood flow by mesenteric left portal vein bypass (MLPVB) improved it. DESIGN: Twelve children with EHPVT and no overt PSE underwent comprehensive neurocognitive testing before and 1 year after undergoing surgery with intent to perform MLPVB. The evaluations sampled 4 functional domains at both time points: (1) neurobehavioral (behavior, emotional, executive functioning); (2) broad cognitive (intelligence, achievement); (3) fluid ability (attention, mental speed, working memory, memory encoding); and (4) visual motor (drawing, fine motor). Tasks in the fluid-ability and visual-motor domains were expected to be especially sensitive to adverse effects of EHPVT and to be most likely to show improvement with MLPVB. The test group consisted of 8 subjects who underwent successful MLPVB, and the comparison group was composed of 3 patients who received distal splenorenal shunts and one whose MLPVB failed. RESULTS: Both groups demonstrated similar fluid cognitive ability at initial evaluation. Successful MLPVB resulted in significantly improved fluid cognitive function: in the fluid cognitive domain, significant improvements were seen for the hit reaction time variability in the Conner's Continuous Performance Test, the attention scale of the Cognitive Assessment System, and immediate verbal memory in the Children's Memory Scale. In the visual-motor domain, z scores on the Grooved Pegboard Test improved. No improvement was observed in the comparison group. DISCUSSION: The results show that surgically restoring portal flow to the liver in children with primary EHPVT results in improved fluid cognitive ability. Subjects showed some neurocognitive abnormalities involving mainly fluid cognitive ability consistent with minimal PSE seen in adults with chronic liver disease. Cognitive defects in patients with minimal PSE seem to relate primarily to attention and fine motor skill, and although affected patients can function in everyday life, they are at risk for performance deficits in educational and vocational situations requiring the ability to pay close attention and react quickly (eg, driving, employment in manufacturing). The tests we administered in these domains are pediatric equivalents to measures used to detect minimal PSE in adults and should detect abnormalities in the same functional domains. Our results suggest that a narrow battery of tests could be used to detect minimal PSE in children in a manner similar to the 5-test battery used in adults, eliminating the need for the comprehensive and broad testing we performed. Our findings suggest that shunting of portal blood from the liver in primary EHPVT can result in PSE and question whether it is as benign a disease as previously thought. The importance of our findings is twofold. For understanding the pathophysiology of PSE, we have shown that restoring blood flow to the liver improves cognitive function in children with EHPVT. For therapy for EHPVT, it becomes clear that MLPVB is an excellent treatment option. It is effective for treating the complications of portal hypertension and provides effective portal blood flow that other medical and surgical therapies do not. The findings provide additional evidence that primary EHPVT should be considered curable by MLPVB. However, comparison of overall risks and benefits of MLPVB with those of other therapeutic options and longer-term outcome studies must be completed before MLPVB can be fully endorsed as the best treatment for EHPVT in children. CONCLUSIONS: Surgical restoration of portal venous flow to the liver in children with primary EHPVT by MLPVB improves fluid cognitive ability. MLPVB should be considered in treating primary EHPVT, because it corrects portal blood flow and could optimize learning potential.

Anastomosis, Surgical↗
PubMed2005

Liver graft volume estimation in 100 living donors: measure twice, cut once.

Estimation of graft volume (GV) is critical in living donor liver transplantation. This study examines the accuracy of formula-derived GV estimates and compares them to both radiogically-derived estimates and actual measurements. We first compared formula-derived estimates of GV and compared them to actual volumes to provide estimates for both right lobe (RL) and left lateral segment (LLS) GV. We then applied these formulae to a validation cohort. Finally, we evaluated both formula-derived and radiologically-derived estimates by comparing them to actual GV measurements. There is a marginal concordance between formula-derived calculation and GV for RL donors, but the error ratio was lower than for radiologic estimates. In contrast, MRI measurements for LLS grafts demonstrated a lower error ratio than formula-derived estimation. Formula-derived estimates of GV should be routinely used in the initial screening of potential living donors as long as their limitations are appreciated.

Biometry↗
PubMed2005

Selection for acute liver failure: have we got it right?

1. The interplay of four factors determines the outcome in Acute Liver Failure (ALF). Current criteria used for prognosis address each of these factors. a. Hepatic regeneration: Age, poor prognostic etiologies (drug, idiopathic ALF), b. Hepatocellular failure: INR, Bilirubin, c. Encephalopathy and brain edema: Stage III/IV, hyperacute vs acute/subacute, d. Multiorgan failure (MOF): pH. 2. In hyperacute liver failure, exemplified by acetaminophen-induced injury, prognostic criteria have focused on the course of encephalopathy and of multiorgan failure. In non-acetaminophen induced ALF, prognostic criteria reflect a greater role of hepatic regeneration in outcome. 3. Prognostic indices combine features of these four factors. The Kings College criteria (KCC) have been shown to have a better performance than the Clichy criteria. The KCC appear to have a higher specificity than sensitivity for acetaminophen-induced ALF, while its negative predictive value for non-acetaminophen induced ALF is unfortunately low. 4. Newer prognostic markers have been proposed, including serum phosphate and alpha fetoprotein as markers of regeneration and blood lactate, a reflection of MOF and hepatocellular failure. They are likely to complement the KCC rather than replace them. 5. Clinical judgement is still needed to weigh management options in this disease.

Biomarkers↗
PubMed2005

Complications and use of intracranial pressure monitoring in patients with acute liver failure and severe encephalopathy.

Monitoring of intracranial pressure (ICP) in acute liver failure (ALF) is controversial as a result of the reported complication risk (approximately 20%) and limited therapeutic options for intracranial hypertension. Using prospectively collected information from 332 patients with ALF and severe encephalopathy, we evaluated a recent experience with ICP monitoring in the 24 centers constituting the U.S. ALF Study Group. Special attention was given to the rate of complications, changes in management, and outcome after liver transplantation (LT). ICP monitoring was used in 92 patients (28% of the cohort), but the frequency of monitoring differed between centers (P < 0.001). ICP monitoring was strongly associated with the indication of LT (P < 0.001). A survey performed in a subset of 58 patients with ICP monitoring revealed intracranial hemorrhage in 10.3% of the cohort, half of the complications being incidental radiological findings. However, intracranial bleeding could have contributed to the demise of 2 patients. In subjects listed for LT, ICP monitoring was associated with a higher proportion of subjects receiving vasopressors and ICP-related medications. The 30-day survival post-LT was similar in both monitored and nonmonitored groups (85% vs. 85%). In conclusion, the risk of intracranial hemorrhage following ICP monitoring may have decreased in the last decade, but major complications are still present. In the absence of ICP monitoring, however, patients listed for LT appear to be treated less aggressively for intracranial hypertension. In view of the high 30-day survival rate after LT, future studies of the impact of intracranial hypertension should also focus on long-term neurological recovery from ALF.

Adult↗
PubMed2005

The pathophysiology of brain edema in acute liver failure.

Brain edema leading to intracranial hypertension is a cause of death in acute liver failure (ALF). The pathogenesis of this unique complication has been investigated in man, in experimental models and in isolated cell systems. From this experience, an integrated view has emerged, pointing at several mechanisms that contribute to cerebral swelling; an osmotic derangement in astrocytes, changes in cellular metabolism as well as alterations of cerebral blood flow. The ability of mild hypothermia to counteract each of these changes in experimental systems has supported the organization of a clinical trial of mild cooling in this disease. Such an advance can be viewed as the clinical translation of 20 years of research in this area.

Animals↗
PubMed2005

Mild hypothermia for acute liver failure: a review of mechanisms of action.

Brain edema with intracranial hypertension is a major complication in patients with acute liver failure. Current therapies for this complication include a variety of pharmacologic and interventional measures, some of which are frequently associated with adverse effects or contraindications. Even though these measures usually allow the control of intracranial hypertension for a certain period of time, recurrence is common. New therapies are therefore needed. Increasing clinical and experimental evidence suggests that induction of mild hypothermia (32 degrees C-35 degrees C) may be a therapeutic alternative. Similar to traumatic brain injury or brain stroke, induction of mild hypothermia seems highly effective to reduce intracranial pressure in patients with acute liver failure. Several mechanisms by which mild hypothermia may prevent brain edema and intracranial hypertension in this condition have been disclosed and may include beneficial effects on ammonia metabolism, as well as on the disturbances of brain osmolarity, cerebrovascular hemodynamics, brain glucose metabolism, inflammation, and others. Improvement of systemic hemodynamics and amelioration of liver injury may be other benefits of the systemic induction of mild hypothermia, but the impact of potential adverse events, such as infection, should also be taken into account. At a time when mild hypothermia is increasingly used in several specialized centers, performance of a randomized controlled trial seems critical to confirm the benefits of mild hypothermia in acute liver failure and to provide adequate guidelines for its use.

Ammonia↗
PubMed2004

Comparative analysis of live liver donation risk using a comprehensive grading system for severity.

We investigated whether right lobe (RL) liver donation is associated with a higher incidence or severity of donor complications than left lobe (LL) liver and left lateral segment (LLS) liver donations. We studied 80 living donors: 35 RL liver donors and 45 LL/LLS liver donors. A modification of the Clavien classification was used to grade the severity of complications. RL and LL/LLS liver donations had equivalent blood loss, readmission and reoperation rates, use of blood products, and lengths of stay in the intensive care unit and hospital. RL liver donors underwent longer surgeries and experienced more postoperative pain than LL/LLS liver donors. The overall rate of complications was 33%. There was a higher rate of complications in RL liver donors (51%) than LL/LLS liver donors (20%). When graded by severity, there were more grade 2 complications in RL liver donors than in LL/LLS liver donors. Our report confirms that RL liver donation is associated with higher morbidity than LL/LLS liver donation. When the complications are systematically graded by severity, there is a significant difference in Clavien grade 2 complications in RL liver donors.

Adult↗
PubMed2004

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Clinical Trials as Topic↗
PubMed2004

Cerebral blood flow in acute liver failure: a finding in search of a mechanism.

In the last few years, several abnormalities of cerebral blood flow (CBF), namely loss of cerebral autoregulation, altered reactivity to carbon dioxide, and development of cerebral hyperemia, have been described in patients as well as experimental models of acute liver failure (ALF) and/or hyperammonemia. The development of cerebral hyperemia seems particularly relevant to the pathogenesis of brain edema in ALF. In addition to the potential increase of brain blood volume causing a rise in intracranial pressure, an increase of CBF could facilitate the movement of water across the blood brain barrier in an osmotically altered brain. Because maneuvers that abrogate the rise of CBF have been shown to prevent or ameliorate brain edema in ALF/hyperammonemia, elucidation of the mechanism by which the rise of CBF occurs is important. In the rat after portacaval anastomosis receiving an ammonia infusion, the signal resulting in cerebral hyperemia arises within the brain once maximal glutamine accumulation has occurred in astrocytes. Several mediators potentially involved in the development of cerebral hyperemia in ALF are examined in this review, but further work is needed to assess the role, if any, of each of them.

Animals↗